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. 2022 Oct 26;15(3):765–795. doi: 10.1016/j.jcmgh.2022.10.014

Figure 9.

Figure 9

The microbiome regulates systemic levels of indole-3-propionic acid (IPA), colonic PXR signaling, and responsiveness of myofibroblasts to inflammatory stimuli. (A) Schematic showing the conversion pathway of tryptophan into different bioactive indole metabolites including those that require the gut microbiota for conversion. (B) Serum levels of tryptophan (trp) and the tryptophan metabolites indole-3-acetic acid (IAA), indole-3-lactic acid (ILA), and indole-3-propionic acid (IPA) in specific pathogen–free (SPF), antibiotic-administered (ABX), and germ-free (GF) mice (expressed as fold-change relative to SPF control; n = 4–5 per group). (C) Expression of the PXR target gene Cyp3a11 as measured by quantitative polymerase chain reaction in the colon of SPF, ABX, and GF mice (n = 4–8 per group). (D) Gene expression of inflammatory mediators in myofibroblasts isolated from the colon of SPF and GF mice and stimulated with LPS or cytomix (cyto) for 12 hours (n = 3 per group). (E) Gene expression of inflammatory mediators in myofibroblasts isolated from the colon of WT mice administered normal drinking water or drinking water supplemented with IPA (pH matched) for 2 weeks and then stimulated with LPS for 12 hours (n = 3 per group). One-way analysis of variance with Tukey post hoc test (B–E). ∗P < .05, ∗∗P < .01, ∗∗∗P < .001.